Objective. To find molecular markers for the diagnosis of acute myocardial infarction (AMI), this research further verified the relationship between the expression level of FFAR2 gene and AMI by expanding the sample size based on the previous gene chip results. Methods. Peripheral venous leukocytes were collected from 113 patients with AMI and 94 patients with noncoronary artery disease as the experimental group and the control group, respectively. Real-time fluorescence quantitative polymerase chain reaction was used to detect the expression of the FFAR2 gene. Western blot analysis was applied to detect the relative expression of the FFAR2 gene at the level of protein. Furthermore, the relationship between gene expression and clinical data was also analyzed and compared. Results. The level of expression of FFAR2 gene in peripheral blood of patients with AMI was significantly lower than that of the control group (0.33 [0.04–1.08], 0.62 [0.07–1.86], respectively; p<0.05), which was 0.53 times that of the control group. Western blot results presented that the FFAR2 protein level in the peripheral blood of the AMI group was lower than that of the control group (0.114; p=0.004). Analyzing clinical data of the subjects indicated that the average age of the AMI group was significantly higher than the age of control group (p<0.01). Also, the fasting blood glucose level was higher (p<0.01), and the high-density lipoprotein cholesterol (HDL-C) level was lower (p=0.03). The FFAR2 mRNA level correlated positively with the HDL-C level (p<0.01). Logistic regression analysis suggested that the low expression of the FFAR2 gene in peripheral blood may be a risk factor for AMI independent of age, family history of diabetes, fasting blood glucose level, and HDL-C level (p=0.025). Compared with the high FFAR2 expression group, the risk of AMI in the low FFAR2 expression group was 6.308 times higher. Conclusion. The expression level of the FFAR2 gene in peripheral blood of patients with AMI was significantly lower than that in the control group. Low expression of the FFAR2 gene in peripheral blood is an independent risk factor for AMI. Hence, it may also be a potential biomarker to predict AMI.

Objective This study aimed to investigate whether differential expression of the retinoic acid receptor-related orphan receptor A ( RORA) gene is related to occurrence of acute myocardial infarction (AMI). Methods This was a retrospective study. White blood cells of 93 patients with acute myocardial infarction and 74 patients with stable coronary artery disease were collected. Reverse transcription quantitative polymerase chain reaction and western blotting were used to measure RORA mRNA and protein expression, respectively. Results RORA mRNA expression levels in peripheral blood leukocytes in patients with AMI were 1.57 times higher than those in patients with stable coronary artery disease. Protein RORA levels in peripheral blood of patients with AMI were increased. Binary logistic regression analysis showed that high expression of RORA was an independent risk factor for AMI, and it increased the risk of AMI by 2.990 times. Conclusion RORA expression levels in patients with AMI is significantly higher than that in patients with stable coronary artery disease. High expression of RORA is related to AMI and it may be an independent risk factor for AMI.

Purpose ZCCHC9 is a zinc finger protein with a CCHC zinc finger structure and has important roles in several cellular processes. This study was conducted on an expanded number of samples to evaluate The usefulness of ZCCHC9 gene expression in peripheral blood as a molecular marker for the prediction of AMI (acute myocardial infarction) risk. Patients and Methods Peripheral blood samples were collected from 117 patients with stable CAD (coronary atherosclerotic disease) and 126 patients with AMI. The mRNA level of the ZCCHC9 gene was assessed by qRT-PCR, and its protein level was determined by Western blotting. Results The AMI group exhibited reduced expression of the ZCCHC9 gene, at both transcript and protein levels, than the stable CAD group. The low expression of the ZCCHC9 gene was not related to blood glucose level (P=0.635), blood lipid level, and troponin level (P=0.715), and may cause AMI through the MAPK signaling pathway. Compared with other patients, patients with low ZCCHC9 gene expression in their peripheral blood have a 2.597-fold higher risk of AMI. Conclusion ZCCHC9 gene expression in peripheral blood was significantly lower in patients with AMI than in stable CAD patients. Individuals with low expression of ZCCHC9 in peripheral blood have higher a probability to develop AMI than those with stable CAD. Thus, lowered ZCCHC9 gene expression can act as an independent risk factor for AMI.